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低碳酸血症时延髓“前包钦格复合体”区域呼吸神经元活动的改变

Alterations in respiratory neuronal activities in the medullary 'pre-Bötzinger' region in hypocapnia.

作者信息

St-John W M

机构信息

Department of Physiology, Dartmouth-Hitchcock, Medical Center, Dartmouth Medical School, Lebanon, NH 03756-0001, USA.

出版信息

Respir Physiol. 1998 Nov;114(2):119-31. doi: 10.1016/s0034-5687(98)00088-7.

Abstract

'Pre-inspiratory' neuronal activities in a rostral ventrolateral medullary 'pre-Bötzinger' complex have been hypothesized to generate eupnea. Respiratory-modulated neuronal activities were recorded in this region in decerebrate, vagotomized, paralyzed, and ventilated cats, having bilateral carotid sinus nerve sections. As end-tidal partial pressures of carbon dioxide were reduced to hypocapnic levels, all neuronal activities which were tonic or expiratory inspiratory ('pre-inspiratory') either ceased or lost respiratory-modulation. Similarly, most expiratory and inspiratory expiratory activities did not maintain a phasic discharge. Half of the inspiratory neuronal activities did continue a phasic discharge, which commenced after phrenic activity or became independent of the phrenic rhythm. Results do not support a fundamental role of the 'pre-Bötzinger' complex in the neurogenesis of eupnea. Some neuronal activities can establish a phasic discharge in hypocapnia which is independent of the central respiratory rhythm. At normocapnia, this independent discharge is superseded and incorporated into the ponto-medullary respiratory neuronal circuit which generates eupnea.

摘要

延髓头端腹外侧部“前包钦格复合体”中的“吸气前”神经元活动被认为可产生平静呼吸。在双侧切断颈动脉窦神经的去大脑、迷走神经切断、麻痹且通气的猫的该区域记录到了呼吸调制的神经元活动。随着呼气末二氧化碳分压降至低碳酸血症水平,所有呈紧张性或呼气性吸气性(“吸气前”)的神经元活动要么停止,要么失去呼吸调制。同样,大多数呼气性和吸气性呼气活动也未维持相位性放电。一半的吸气性神经元活动确实继续呈相位性放电,这种放电在膈神经活动之后开始,或者变得与膈神经节律无关。结果不支持“前包钦格复合体”在平静呼吸神经发生中起基本作用的观点。一些神经元活动可在低碳酸血症时建立与中枢呼吸节律无关的相位性放电。在正常碳酸血症时,这种独立放电被取代并纳入产生平静呼吸的脑桥 - 延髓呼吸神经元回路。

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